PRMT2 silencing regulates macrophage polarization through activation of STAT1 or inhibition of STAT6

Ting Liu1, Yinjiao Li1, Muqiu Xu1

  • 1Department of Anesthesiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

BMC Immunology
|January 3, 2024
PubMed
Abstract

Insights

Protein arginine methyltransferase 2 (PRMT2) influences macrophage polarization. Silencing PRMT2 promotes M1 macrophage markers via STAT1 activation and reduces M2 markers by inhibiting STAT6.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Macrophages are key innate immune cells, exhibiting M1 (pro-inflammatory) and M2 (anti-inflammatory) polarization.
  • Protein arginine methyltransferase 2 (PRMT2) is implicated in inflammatory processes.
  • The specific role of PRMT2 in M1/M2 macrophage polarization remains largely uncharacterized.

Purpose of the Study:

  • To investigate the effect of PRMT2 on macrophage polarization.
  • To elucidate the underlying molecular mechanisms by which PRMT2 influences M1/M2 macrophage phenotypes.

Main Methods:

  • Bone marrow-derived macrophages (BMDMs) were differentiated and polarized into M1 or M2 states.
  • Stimuli included lipopolysaccharide (LPS) with interferon-gamma (IFN-γ) for M1, and interleukin-4 (IL-4) for M2 polarization.
  • Techniques employed were quantitative polymerase chain reaction (qPCR), western blot, and flow cytometry (FCM) to assess markers and signaling pathways.

Main Results:

  • PRMT2 expression was significantly upregulated in M1 macrophages induced by LPS/IFN-γ, with minimal change in M2 macrophages induced by IL-4.
  • Knockdown of PRMT2 enhanced M1 macrophage markers, correlating with STAT1 activation.
  • PRMT2 knockdown also decreased M2 macrophage markers, associated with STAT6 inhibition.

Conclusions:

  • PRMT2 plays a crucial role in modulating macrophage polarization.
  • PRMT2 silencing promotes M1 polarization by activating STAT1.
  • PRMT2 inhibition of STAT6 contributes to the attenuation of the M2 macrophage state.